S. pneumoniae is one of the most common causes of bacterial meningitis in adults and young adults, along with Neisseria meningitidis, and is the leading cause of bacterial meningitis in adults in the USA. It is also one of the top two isolates found in ear infection, otitis media.[3] Pneumococcal pneumonia is more common in the very young and the very old.

The organism was termed Diplococcus pneumoniae from 1920[6] because of its characteristic appearance in Gram-stainedsputum. It was renamed Streptococcus pneumoniae in 1974 because of its growth in chains in liquid growth media.

The genome of S. pneumoniae is a closed, circular DNA structure that contains between 2.0 and 2.1 million base pairs, depending on the strain. It has a core set of 1553 genes, plus 154 genes in its virulome, which contribute to virulence, and 176 genes that maintain a noninvasive phenotype. Genetic information can vary up to 10% between strains.[9]

Natural bacterial transformation involves the transfer of DNA from one bacterium to another through the surrounding medium. Transformation is a complex, developmental process requiring energy, dependent on expression of numerous genes. In S. pneumoniae at least 23 genes are required. In order for a bacterium to bind, take up and recombine exogenous DNA into its chromosome it must enter a special physiological state, called competence.

Competence, in S. pneumoniae, is induced by DNA-damaging agents such as mitomycin C, a DNA inter-strand cross-linking agent, and the fluoroquinoloneantibioticsnorfloxacin, levofloxacin and moxifloxacin, topoisomerase inhibitors that cause double-strand breaks.[10] Transformation protects S. pneumoniae against the bactericidal effect of mitomycin C.[11] Michod et al.[12] summarized evidence that induction of competence in S. pneumoniae is associated with increased resistance to oxidative stress and increased expression of the RecA protein, a key component of the recombinational repair machinery for removing DNA damages. On the basis of these findings, they suggested that transformation is an adaptation for repairing oxidative DNA damages. S. pneumoniae infection stimulates polymorphonuclear leukocytes (granulocyte) to produce an oxidative burst that is potentially lethal to the bacteria. The ability of S. pneumoniae to repair the oxidative DNA damages in its genome, caused by this host defense, likely contributes to this pathogen’s virulence.

When both bacteria are placed together into the nasal cavity of a mouse, within 2 weeks, only H. influenzae survives. When both are placed separately into a nasal cavity, each one survives. Upon examining the upper respiratory tissue from mice exposed to both bacteria, an extraordinarily large number of neutrophil immune cells were found. In mice exposed to only one bacterium, the cells were not present.

Lab tests show neutrophils that were exposed to already-dead H. influenzae were more aggressive in attacking S. pneumoniae than unexposed neutrophils. Exposure to killed H. influenzae had no effect on live H. influenzae.

Two scenarios may be responsible for this response:

When H. influenzae is attacked by S. pneumoniae, it signals the immune system to attack the S. pneumoniae

The combination of the two species sets off an immune system alarm that is not set off by either species individually.

It is unclear why H. influenzae is not affected by the immune system response.[14]

Diagnosis is generally made based on clinical suspicion along with a positive culture from a sample from virtually any place in the body. An ASO Titre of >200 units is significant. [2]S. pneumoniae is, in general, optochin sensitive, although optochin resistance has been observed.[15]

^Sternberg, George Miller (30 April 1881). "A fatal form of septicaemia in the rabbit produced by the subcutaneous injection of human saliva. An experimental research". Bulletin of the National Board of Health (Baltimore, Maryland).

^Winslow, C., and J. Broadhurst (1920). "The Families and Genera of the Bacteria: Final Report of the Committee of the Society of American Bacteriologists on Characterization and Classification of Bacterial Types". J Bacteriol5 (3): 191–229. PMC378870. PMID16558872.